miR-29b suppresses proliferation and induces apoptosis of hepatocellular carcinoma ascites H22 cells via regulating TGF-β1 and p53 signaling pathway

MicroRNA (miR)-29b is a key tumor regulator. It can inhibit tumor cell proliferation, induce apoptosis, suppress tumor invasion and migration, thus delaying tumor progression. Our previous studies revealed an increased level of miR-29b in hepatoma 22 (H22) cells in ascites tumor-bearing mice. The present study investigated the effect of miR-29b on proliferation and apoptosis of hepatocellular carcinoma ascites H22 cells and its association with the transforming growth factor-β1 (TGF-β1) signaling pathway and p53-mediated apoptotic pathway. Briefly, H22 cells were transfected with miR-29b-3p (hereinafter referred to as miR-29b) mimic or miR-29b inhibitor. MTS cell proliferation assay and flow cytometry were used to analyze cell viability and apoptosis. The expression change of the TGF-β1 signaling pathway and p53-mediated apoptotic pathway were detected by reverse transcription-quantitative PCR, western blotting and immunofluorescence. Furthermore, cells were treated with exogenous TGF-β1 and TGF-β1 small interfering RNA to evaluate the crosstalk between TGF-β1 and p53 under miR-29b regulation. The overexpression of miR-29b decreased cell viability, increased cell apoptosis, activated the TGF-β1 signaling pathway and p53-mediated apoptotic pathway. Conversely, these effects were reversed by the miR-29b inhibitor. Moreover, the effect of miR-29b mimic was further increased after treating cells with exogenous TGF-β1. The activation of the TGF-β1 signaling pathway and p53-mediated apoptotic pathway induced by miR-29b overexpression were reversed by TGF-β1 inhibition. In summary, these data indicated that miR-29b has an important role in proliferation and apoptosis of H22 cells by regulating the TGF-β1 signaling pathway, the p53-dependent apoptotic pathway, and the crosstalk between TGF-β1 and p53.